The innate immune response, in which a signal such as amyloid β, asbestos, urate crystals, cholesterol crystals, or oligomers of islet amyloid polypeptides triggers formation of complexes called inflammasomes containing NLRP3, an adaptor protein ASC and caspase-1, followed by activation of caspase-1, leading to production of IL-1β, is considered to be one of the causes of Alzheimer's disease, asbestosis, gout, arteriosclerosis, type 2 diabetes and the like (Halle A, et al., Nat Immunol. 9:857-65, 2008; Dostert C, et al., Science vol. 320, pp. 674-677, 2008; Peter D, et al., Nature 464: 1357-1361, 2010; Martinon F, et al., Nature 440:237-41, 2006; Masters SL, et al., Nat Immunol. 11:897-904, 2010).
On the other hand, CINCA (Chronic Infantile Neurologic Cutaneous and Articular) syndrome is one of autoinflammatory syndromes and about a half of patients suffering from this syndrome have a heterozygous mutation in the NLRP3 gene. This mutant NLRP3 gene is said to cause systemic inflammation by constantly activating the above-described inflammasomes.
However, a screening system suitable for developing drugs for suppressing an activity of inflammasome containing NLRP3, which is common among these diseases, has not yet been developed.